2017
Loss of the podocyte glucocorticoid receptor exacerbates proteinuria after injury
Zhou H, Tian X, Tufro A, Moeckel G, Ishibe S, Goodwin J. Loss of the podocyte glucocorticoid receptor exacerbates proteinuria after injury. Scientific Reports 2017, 7: 9833. PMID: 28852159, PMCID: PMC5575043, DOI: 10.1038/s41598-017-10490-z.Peer-Reviewed Original ResearchConceptsKnockout miceGlucocorticoid receptorNephrotic syndromeSimilar renal functionMainstay of therapyReceptor knockout miceTreatment of proteinuriaFoot process effacementMechanism of actionImmunomodulatory therapyRenal functionGlomerular injuryProtein excretionKO miceCommon disorderNephrotoxic serumPodocyte injuryPodocyte-specific deletionMouse modelSlit diaphragm proteinsWild-type podocytesProcess effacementProteinuriaUnstimulated conditionsKnockout animals
2009
Resolution of renal inflammation: a new role for NF-κB1 (p50) in inflammatory kidney diseases
Panzer U, Steinmetz OM, Turner JE, Meyer-Schwesinger C, von Ruffer C, Meyer TN, Zahner G, Gómez-Guerrero C, Schmid RM, Helmchen U, Moeckel GW, Wolf G, Stahl RA, Thaiss F. Resolution of renal inflammation: a new role for NF-κB1 (p50) in inflammatory kidney diseases. American Journal Of Physiology. Renal Physiology 2009, 297: f429-f439. PMID: 19458123, DOI: 10.1152/ajprenal.90435.2008.Peer-Reviewed Original ResearchMeSH KeywordsActive Transport, Cell NucleusAcute DiseaseAnimalsAntilymphocyte SerumBlotting, SouthwesternCells, CulturedChemokinesDisease Models, AnimalEndothelial CellsGlomerulonephritisImmunohistochemistryKidney GlomerulusLipopolysaccharidesMaleMiceMice, Inbred C57BLMice, KnockoutNephritisNF-kappa B p50 SubunitNF-kappa B p52 SubunitProtein MultimerizationRatsRats, WistarRemission, SpontaneousTime FactorsTranscription Factor RelATranscription Factor RelBConceptsNF-kappaBRenal inflammationTissue injuryNF-kappaB p50 knockout miceRenal inflammatory cell infiltrationHighest chemokine expressionP50 knockout miceRenal tissue injuryResolution of LPSGlomerular immune injuryInflammatory kidney diseasesInflammatory cell infiltrationRenal inflammatory diseaseProinflammatory gene expressionModel of glomerulonephritisTranscription factor NF-kappaBResolution periodImmune injuryRenal diseaseChemokine expressionAcute nephritisKidney diseaseCell infiltrationInflammatory diseasesInflammatory process